Mean platelet volume and its relationship with carotid atherosclerosis in subjects with non-alcoholic fatty liver disease.

BACKGROUND: Non-alcoholic fatty liver disease (NAFLD) is linked to an increased risk of cardiovascular disease. Mean platelet volume (MPV), a determinant of platelet activation, is an emerging risk factor for atherothrombosis. AIMS: The aim of this study was to investigate the levels of MPV in subjects with NAFLD having no confounding factors for atherosclerosis such as obesity, diabetes mellitus, and hypertension. In addition, the possible relationship between MPV and carotid artery intima media thickness (CIMT), a well known marker of subclinical atherosclerosis, was also studied. METHODS: MPV and CIMT levels were measured in 60 biopsy-proven NAFLD subjects and 54 healthy controls. Age and sex were similar between two groups. RESULTS: Body mass index and waist circumference levels were higher in the NAFLD group when compared to the controls. There were no differences between the two groups regarding LDL cholesterol levels, whereas HDL cholesterol levels were lower in the NAFLD group. MPV and CIMT levels were not different between the two groups. According to the correlation analyses, CIMT levels were positively correlated to age in patients with NAFLD. However, no significant correlation was found between MPV and CIMT levels. CONCLUSIONS: The results of this study do not show any difference in MPV levels between subjects with NAFLD and controls. These finding suggests that in the absence of other metabolic risk factors, MPV might not be involved in the mechanism(s) of increased cardiovascular risk in NAFLD.

Circulating levels of interleukin-18 in patients with non-alcoholic fatty liver disease.

BACKGROUND AND AIMS: Non-alcoholic fatty liver disease (NAFLD) is strongly associated with obesity and diabetes mellitus. IL-18 is associated with obesity and metabolic syndrome. Our aim was to investigate the relationship of IL-18 with adiponectin and liver histology in subjects with NAFLD who had no additional disorder such as morbid obesity, diabetes mellitus and hypertension. METHODS: Plasma levels of IL-18 and adiponectin were measured by ELISA in 96 male subjects with NAFLD [n = 65 for non-alcoholic steatohepatitis (NASH) and n = 31 for simple steatosis (SS)]. RESULTS: IL-18 levels were not different between the two groups (p = 0.89). There was no significant association of IL-18 with adiponectin, insulin resistance and histopathological findings. Adiponectin was lower in the NASH group compared to the SS group (p = 0.02) and it was found to be negatively correlated with hepatic steatosis and fibrosis (r = -0.442, p < 0.001 and r = -0.292, p = 0.02, respectively). CONCLUSIONS: This study indicates that circulating IL-18 levels are not altered in male subjects with NAFLD. These results suggest that in the absence of metabolic risk factors, IL-18 per se may not be involved in the pathogenesis of NASH and SS.

Decreased oxidation susceptibility of plasma low density lipoproteins in patients with Gilbert's syndrome.

BACKGROUND AND AIM: The association of hyperbilirubinemia in Gilbert's syndrome (GS) with a decrease in prevalence of coronary artery disease is a well-known phenomenon. In this study, the state of low-density lipoprotein (LDL) oxidation which has been postulated to be a significant determinant at the etiopathogenesis of atherosclerotic disorders was investigated among individuals with GS. METHODS: For this purpose, serum cholesterol, LDL cholesterol, high-density lipoprotein cholesterol, triglycerides, uric acid, apolipoprotein A and B, bilirubins, thiobarbituric acid-reactive substances, and the sensitivity of LDL oxidation levels, as well as serum alanine aminotransferase, aspartate aminotranserfase, gamma glutamyl transferase, and alkaline phosphatase activities, were determined in 17 patients with Gilbert's syndrome and 15 healthy adults. RESULTS: There was no significant difference between the groups except the indirect bilirubin parameter (P < 0.001). In comparison with the healthy individuals, LDL oxidation levels between 75 and 120 min were significantly lower (P < 0.005) along with prolonged lag-phase in GS patients, indicating a delay in oxidation susceptibility. CONCLUSION: It is suggested that the chronic hyperbilirubinemia leading to a lag-phase prolongation in LDL oxidation and a decrease in LDL oxidation may be reason for the low percentage of coronary artery disease.

Levels of serologic markers of celiac disease in patients with reflux esophagitis.

AIM: To investigate the prevalence of celiac disease serologic markers (antigliadin IgA, IgG, and anti-endomysial IgA) in patients with reflux esophagitis and to detect the relationship between reflux esophagitis and celiac disease (CD). METHODS: This study was performed prospectively between January 2003 and January 2004. Sixty-eight adult reflux esophagitis patients and 40 people as control group for symptoms related with gastrointestinal system were enrolled in this study. The diagnostic work-up included an accurate medical history with gastrointestinal symptoms, routine laboratory measurements, the detection of antibodies against gliadin (IgA and IgG) and endomysium (IgA), and an upper endoscopy with postbulbar biopsy. RESULTS: IgA-AGA and IgG-AGA were positive at 8.8% and 10.3% in patients with reflux esophagitis. In control group, it was found that 10% people had positive IgA-AGA, and 7.5% people had positive IgG-AGA. There was no significant relationship between patients and control group regarding positive IgA-AGA and IgG-AGA. The patients and persons in control group had no positive IgA-EMA. On postbulbar biopsies, no finding was detected concerning celiac disease. There were no symptoms and signs for gluten enteropathy in patients and control group. CONCLUSION: This review supports that an association does not exist between celiac disease and reflux esophagitis. We think these diseases exist independently from each other.

Elevated plasma homocysteine concentrations as a predictor of steatohepatitis in patients with non-alcoholic fatty liver disease.

BACKGROUND: Although steatosis is common in patients with severe hyperhomocysteinemia due to deficiency of cystathionine beta-synthase, there are no satisfactory data on homocysteine concentrations in patients with non-alcoholic fatty liver disease. The main aim of the present study was to evaluate the clinical significance of plasma homocysteine concentrations in patients with non-alcoholic fatty liver disease. METHODS: Seventy-one non-alcoholic fatty liver disease patients, 36 patients with chronic viral hepatitis and 30 healthy persons were enrolled in the study. Homocysteine levels were measured by high-performance liquid chromatography. Insulin, folate, vitamin B(12) and lipoprotein levels were also determined in all groups. RESULTS: Homocysteine in the non-alcoholic fatty liver disease group was found to be significantly higher than other groups. Homocysteine was found to be significantly higher in the non-alcoholic steatohepatitis group when compared with simple steatosis group. A positive correlation was found between homocysteine and triglyceride, very-low-density-lipoprotein (VLDL) cholesterol, insulin, and index of insulin resistance in the non-alcoholic fatty liver disease group, and a negative correlation was found between homocysteine and folate, or vitamin B(12) in all groups. The homocysteine threshold for the prediction of steatohepatitis was 11.935 ng/mL. Furthermore; plasma homocysteine was a statistically significant predictor for severity of necroinflammatory activity in non-alcoholic steatohepatitis. CONCLUSIONS: The plasma homocysteine concentrations were significantly higher in patients with non-alcoholic fatty liver disease, while the concentrations were not affected by chronic viral hepatitis. Plasma homocysteine is a parameter for discriminating steatohepatitis from simple steatosis. Determining the plasma homocysteine concentrations may facilitate selection of steatosis patients in whom a liver biopsy should be performed.